Heparin-Induced Thrombocytopenia

Brieger, David; Mak, Koon Hou; Kottke‐Marchant, Kandice; Topol, Eric J.

doi:10.1016/s0735-1097(98)00134-x

Cited by 182 publications

(166 citation statements)

References 117 publications

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“…HIT occurs due to the formation of antibodies against heparin-PF4 complex (the negatively charged heparin polysaccharide molecules bind to positively charged protein tetramer, PF4 to form a complex), which cause platelet activation, leading to thrombosis [8,9] . Immune mediated HIT is diagnosed by 50% drop in platelet count occurring after 4-15 days of heparin therapy [10,11] . It is caused by binding of antibodies to Fcγ receptor present on platelets thereby activating them.…”

Section: Introductionmentioning

confidence: 99%

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

Kannan¹,

Ahmad²,

Ahmad³

et al. 2005

American J. of Immunology

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Abstract:We did the pilot study, in an attempt to determine the prevalence of HIT in Indians and determine its relationship, if any, to FcγRIIa polymorphism, the occurrence of heparin-induced thrombocytopenia (HIT) was investigated in 33 Indian patients undergoing cardiovascular surgery (CVS) who received unfractionated heparin (UFH). Platelet counts were performed prior to the initiation of UFH therapy and 5-16 days, post-therapy. The fall in patients' platelet count >35% of the baseline value or <100,000 µL 1 was considered to be suggestive of HIT syndrome. Heparin-induced platelet aggregation (HIPA), Enzyme Linked Immunosorbant assay (ELISA) and Serotonin Release Assay (SRA) tests were performed in all the patients to detect the antibodies formed against the heparin and platelet factor 4 complex (H-PF4). DNA analysis for FcγRIIa polymorphism was done by allele specific PCR. Thrombocytopenia was found to be present in 10 (30%) patients. Of these, 5 patients were found to be positive by HIPA, ELISA and SRA tests. These 5 patients were considered to have classic HIT syndrome. One of these patients had bleeding while the others were asymptomatic. One of the HIT positive patients was found to be homozygous for FcγRIIa His/ His polymorphism and others were heterozygous, had one defective allele with single amino acid change (Arg 131 His) at FcγRIIa platelet receptor. Frequency of occurrence of homozygous (FcγRIIa His/ His) and heterozygous (FcγRIIa Arg/ His ) polymorphism was higher in patients with HIT (100%) than in the normal population (68%). The prevalence of HIT in the pilot study (15%) was higher than that in the west (5%) but comparable to that from Japan (12%) (14). However, the Occurance of FcγRIIa polymorphism in Indian (68%) was higher than in the east (51%) and comparable to that in the west (78%). Thus it appears that the FcγRIIa polymorphism may have some relation to occurrence of HIT. Higher prevalence of FcγRIIa polymorphism in Indian may predispose to higher prevalence of HIT in India. Thus, it is recommended that, heparin-treated patients should be routinely tested for not only aPTT but also for platelet count, HPF4 antibodies and FcγRIIa polymorphism analysis. From the pilot study, it shows that absence of FcγRIIa receptor polymorphism may suggest low or negligible risk of development of HIT antibodies. However, further studies required with more patients using the same protocol.

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Section: Introductionmentioning

confidence: 99%

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

Kannan¹,

Ahmad²,

Ahmad³

et al. 2005

American J. of Immunology

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“…1-3 Procoagulant effects may be associated with formation of platelet-derived microparticles and/or endothelial activation especially in areas of previous endothelial disruption. [1][2][3] The cornerstone of therapy of HITT is the complete elimination of all sources of heparin exposure. Platelet counts begin to rise 24-48 hours after discontinuation with normalization at 4-7 days.…”

Section: Discussionmentioning

confidence: 99%

“…1-3 Surgery or thrombolytic therapy may be required for limb salvage and other life-threatening situations requiring restoration of blood flow. [1][2][3] Limited pharmacologic treatment options are available and the presence of end-organ dysfunction further increases the complexity and risk of such choices. Warfarin is useful for long-term anticoagulation; however, immediate anticoagulation with warfarin for acute thrombotic events is contraindicated because of an increased risk of thrombosis.…”

Section: Discussionmentioning

confidence: 99%

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Tackling the Devastating Effects of Heparin‐Induced Thrombocytopenia

Abraham

Uber

Lazarchick

et al. 2002

Congestive Heart Failure

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Heparin‐induced thrombocytopenia with associated thrombosis is a potentially catastrophic complication of heparin therapy. Heart failure patients often require heparin therapy in the setting of multiple comorbidities, particularly renal insufficiency. The authors report a case of heparin‐induced thrombocytopenia with associated thrombosis in a patient with multisystem organ failure and discuss dosing regimens using lepirudin for the treatment of this disorder. The potential risk for excessive anticoagulation is highlighted and a conservative dosing strategy with frequent monitoring of this agent in the presence of renal failure is emphasized.

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“…One solution is to equip clottocytes with sensors to detect decreased serum levels of fibrinogen, plasminogen, alpha 2 -antiplasmin, antithrombin III, factor VII, and protein C, and elevated levels of thrombin and various fibrin/fibrinogen-derived degradation products [2i]. If DIC conditions arise, nanorobots might respond by absorbing and metabolizing the excess thrombin (which trigger clotting), or by releasing thrombin inhibitors such as antithrombin III, hirudin, argatroban, or lepirudin [58] or anticoagulants that reduce thrombin generation such as danaparoid [58] to interrupt the cascade [58,59]. For example, a B0.02% Nct concentration of nanorobots, suitably activated according to physician-approved parameters, could replace the entire depleted natural bloodstream content of antithrombin III from onboard stores in seconds.…”

Section: Computational Tasksmentioning

confidence: 99%

Computational Tasks in Medical Nanorobotics

Freitas

2009

Bio‐Inspired and Nanoscale Integrated Computing

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Nanomedicine is the application of nanotechnology to medicine: the preservation and improvement of human health, using molecular tools and molecular knowledge of the human body. Medical nanorobotics is the most powerful form of future nanomedicine technology. Nanorobots may be constructed of diamondoid nanometer-scale parts and mechanical subsystems including onboard sensors, motors, manipulators, power plants, and molecular computers. The presence of onboard nanocomputers would allow in vivo medical nanorobots to perform numerous complex behaviors which must be conditionally executed on at least a semiautonomous basis, guided by receipt of local sensor data and constrained by preprogrammed settings, activity scripts, and event clocking, and further limited by a variety of simultaneously executing real-time control protocols. Such nanorobots cannot yet be manufactured in 2007 but preliminary scaling studies for several classes of medical nanorobots have been published in the literature. These designs are reviewed with an emphasis on the basic computational tasks required in each case, and a summation of the various major computational control functions common to all complex medical nanorobots is extracted from these design examples. Finally, we introduce the concept of nanorobot control protocols which are required to ensure that each nanorobot fully completes its intended mission accurately, safely, and in a timely manner according to plan. Six major classes of nanorobot control protocols have been identified and include operational, biocompatibility, theater, safety, security, and group protocols. Six important subclasses of theater protocols include locational, functional, situational, phenotypic, temporal, and identity control protocols.

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Heparin-Induced Thrombocytopenia

Cited by 182 publications

References 117 publications

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

Tackling the Devastating Effects of Heparin‐Induced Thrombocytopenia

Computational Tasks in Medical Nanorobotics

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